Figure 7. A schematic model illustrating that GPR Q34A peptide inhibits CXCL12/CXCR4-induced TNFα and IL-6 gene expression.

The resulting MUC1 interacts with activated CXCR4 to downregulate TNFα expression (a). Wild-type GPR peptide increased IL-6 expression, but not MUC1 and TNFα expression (b). However, the Q34A peptide increases the anti-inflammatory response (c), thereby regulating the inflammatory microenvironment in the airway.”